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Adjusting the composition of gut microbiota prevents the development of post-stroke depression by regulating the gut-brain axis in mice.
Disturbances in gut microbiota contribute to an imbalanced gut-brain axis, which is critical for post-stroke depression (PSD), while the underlying mechanisms remain unclear. The objective of this study was to examine the effects of modifying gut microbiota through antibiotic treatment (ABX) and fecal microbiota transplantation (FMT) on the progression of PSD. The PSD model was established by occluding the middle cerebral artery (MCAO), followed by a four-week isolated housing and restraint stress initiated three days after MCAO. For ABX, the PSD mice received antibiotic water for four weeks. While another group of PSD mice underwent FMT or fluoxetine (FLX) for four weeks. At day 35 post-MCAO, behavioral tests were conducted. Results indicated ABX and FMT significantly altered the composition of intestinal flora caused by PSD, all the treatments markedly attenuated anxiety- and depressive-like behaviors and inflammation in the gut and brain. ABX obviously alleviated PSD-induced disorder of intestinal barrier, decreased mRNA levels of TNF-α, IL-1β and IL-6, and decreased CD4+ cells in the colon. While FMT significantly decreased CD8+ cells and increased the goblet cells in colon. Furthermore, both ABX and FMT could reduce activated microglia and pro-inflammatory cytokines in the brain, alleviate decreased Nissl's bodies in the hippocampus, and reverse the decreases in 5-HT, Glu and DA in the striatum caused by PSD. Unlike ABX, FMT was similar to FLX. These findings suggest homeostasis of gut microbiota is indispensable for the development of PSD; adjusting the gut microbiota significantly improves PSD with enhanced functions of gut-brain axis.
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Exploring the role of gut microbiota in depression: Pathogenesis and therapeutic insights.
Depression is a common clinical mental disorder characterized by persistent low mood and anhedonia. It has become a major global public health issue due to its complex etiology and unclear mechanisms, resulting in limited diagnostic and therapeutic options. Recent studies indicate that dysbiosis of gut microbiota is closely related to the onset and progression of depression. This article systematically reviews the recent research on the 'microbiota-gut-brain axis' (MGBA), exploring the role and mechanisms of gut microbiota in preclinical and clinical studies. Additionally, it discusses the potential of modulating gut microbiota as a promising therapeutic approach for depression and suggests future research directions, aiming to provide a theoretical basis for research and clinical management of depression.
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An immunometabolic signature of major depressive disorder in systemic lupus erythematosus.
OBJECTIVES: Systemic lupus erythematosus (SLE) frequently affects the central nervous system, leading to neuropsychiatric SLE (NPSLE). Major depressive disorder in SLE (SLEMDD) is the most frequent manifestation of NPSLE and is believed to arise from an immune-mediated process. However, biomarkers for SLEMDD remain lacking. The aim of this study was to identify candidate immunometabolic biomarkers associated with SLEMDD. METHODS: We analysed deep flow cytometry immune phenotyping, gut microbiota profiling, and targeted mass spectrometry-based metabolomics from 99 patients from the LUPIL-2 study (NCT02955615). Biological signatures were identified using unsupervised principal component analysis and supervised decision tree classification. They were then validated in an independent cohort from the TRANSIMMUNOM study (NCT02466217). RESULTS: SLEMDD patients exhibited a distinct immune profile with decreased naïve CD4⁺ T cells and naïve regulatory T cells (Tregs), alongside increased ICOS⁺ effector memory Tregs (94% classification accuracy). Gut microbiota diversity was reduced with depletion of Akkermansia muciniphila and enrichment of Faecalibacterium prausnitzii. Metabolomic analyses revealed disruptions in kynurenine and short-chain fatty acid pathways, including decreased butyrate levels. Integrative analyses demonstrated coordinated alterations linking Treg activation, microbial metabolites, and immune pathways, distinguishing SLEMDD from SLEnon-MDD with up to 85% accuracy. CONCLUSIONS: SLEMDD is associated with an immunometabolic signature involving alterations in Treg phenotype, gut microbiota composition, and metabolic pathways. These findings provide a rationale for future immunoregulatory or microbiota-targeted therapeutic strategies in SLEMDD.
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Feeding Systems and the Gut Microbiome: Gut-Brain Interactions With Relevance to Psychiatric Conditions.
BACKGROUND: Physical and mental health is dependent on the environment, and feeding is a prime example of this environmental exchange. While the hypothalamus controls both feeding behavior and the stress response, the integration of the neural control centers and the peripheral gut allows for disruption in the gastrointestinal systems and dysfunctional communication to the brain. OBJECTIVE: The purpose of this review is to familiarize clinicians with the physiology controlling feeding behavior and its implications for psychiatric conditions, such as anorexia nervosa and depression. Growing understanding of how integrated bacterial life is in the body has shown that gut bacteria regulate basic physiologic processes and are implicated in various disease states and contribute to regulation of mood. Responses to stress have effects on feeding behavior and mood and the regulation of the stress response by the gut microbiota could contribute to the dysfunction seen in patients with psychiatric illnesses. CONCLUSIONS: Gut microbiota may contribute to dysfunction in psychiatric illnesses. New opportunities to modulate existing gut microbiota using probiotics could be novel targets for clinical interventions.
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The intervention of unique plant polysaccharides - Dietary fiber on depression from the gut-brain axis.
As an invisible organ of human body, the gut microbiota plays an important role in human life and has become a hot spot in the field of life science in recent years. Due to the increasing pressure of work and life, people are prone to depression. The in-depth mechanism studies indicated that the gut microbiota could improve the depression symptom through the gut-brain axis (GBA). As unique plant polysaccharides, dietary fiber can effectively modulate the intestinal flora disorders and its crucial role in orchestrating host-microbiota crosstalk has been confirmed. This review highlights the mechanisms that the gut microbiota affects the development of depression through GBA and focuses on dietary fiber intervention on the improvement of intestinal microbiota imbalance, which may provide new ideas for the prevention and treatment of depression.
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Proteomics analysis of the gut-brain axis in a gut microbiota-dysbiosis model of depression.
Major depressive disorder (MDD) is a serious mental illness. Increasing evidence from both animal and human studies suggested that the gut microbiota might be involved in the onset of depression via the gut-brain axis. However, the mechanism in depression remains unclear. To explore the protein changes of the gut-brain axis modulated by gut microbiota, germ-free mice were transplanted with gut microbiota from MDD patients to induce depression-like behaviors. Behavioral tests were performed following fecal microbiota transplantation. A quantitative proteomics approach was used to examine changes in protein expression in the prefrontal cortex (PFC), liver, cecum, and serum. Then differential protein analysis and weighted gene coexpression network analysis were used to identify microbiota-related protein modules. Our results suggested that gut microbiota induced the alteration of protein expression levels in multiple tissues of the gut-brain axis in mice with depression-like phenotype, and these changes of the PFC and liver were model specific compared to chronic stress models. Gene ontology enrichment analysis revealed that the protein changes of the gut-brain axis were involved in a variety of biological functions, including metabolic process and inflammatory response, in which energy metabolism is the core change of the protein network. Our data provide clues for future studies in the gut-brain axis on protein level and deepen the understanding of how gut microbiota cause depression-like behaviors.
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An exploratory study of the gut microbiota in major depression with anxious distress.
OBJECTIVES: To explore differences in the diversity and composition of the gut microbiome between major depressive disorder (MDD) with and without anxious distress. METHODS: The study comprised 117 participants (79 female, 36 male, 2 other, mean age 38.2 ± 13.4 years) with a current major depressive episode (MDE) with (n = 63) and without (n = 54) the anxious distress specifier. A clinical psychologist administered the structured clinical interview for the DSM-5-RV to confirm a diagnosis of depression. Participants provided stool samples which were immediately frozen and stored at -80 °C. These samples were analysed using the Illumina 16S Metagenomics sequencing protocol in which the sequencing primers target the V3 and V4 regions of the 16S rRNA gene. Participants also completed mental health questionnaires to assess severity of depression (BDI-II), generalized anxiety (GAD-7), and stress (PSS). RESULTS: There were no significant group differences in α-diversity (Shannon's diversity Index; Simpson Index), richness (ACE; Chao1), (Pielou's) evenness, or beta diversity (Bray-Curtis dissimilarity index and weighted UniFrac distance) of gut bacteria. Significant group differences in the relative abundance of gut microbiota however were observed at each taxonomical level, including across 15 genera and 18 species. LIMITATIONS: This was an exploratory study that needs to be replicated across larger samples and compared with a healthy control group. CONCLUSIONS: The research contributes to knowledge of the depressive gut microbial profile unique to the anxious distress subtype of MDD.
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Dynamic human gut microbiome and immune shifts during an immersive psychosocial intervention program.
BACKGROUND: Although depression is a leading cause of disability worldwide, the pathophysiological mechanisms underlying this disorder-particularly those involving the gut microbiome-are poorly understood. METHOD: To investigate, we conducted a community-based observational study to explore complex associations between changes in the gut microbiome, cytokine levels, and depression symptoms in 51 participants (Mage = 49.56, SD = 13.31) receiving an immersive psychosocial intervention. A total of 142 multi-omics samples were collected from participants before, during, and three months after the nine-day inquiry-based stress reduction program. RESULTS: Results revealed that depression was associated with both an increased presence of putatively pathogenic bacteria and reduced microbial beta-diversity. Following the intervention, we observed reductions in neuroinflammatory cytokines and improvements in several mental health indicators. Interestingly, participants with a Prevotella-dominant microbiome showed milder symptoms when depressed, along with a more resilient microbiome and more favorable inflammatory cytokine profile, including reduced levels of CXCL-1. CONCLUSIONS: These findings reveal a potentially protective link between the Prevotella-dominant microbiome and depression, as evidenced by a reduced pro-inflammatory environment and fewer depressive symptoms. These insights, coupled with observed improvements in neuroinflammatory markers and mental health from the intervention, may highlight potential avenues for microbiome-targeted therapies for managing depression.
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Exploring the association between urticaria subtypes, anxiety, and depression and potential role of gut microbiota.
AIMS: In observational studies, the causal relationship between urticaria and the risk of psychiatric disorders (anxiety and depression) remains inconclusive. Furthermore, there is growing evidence that gut microbiota (GM) contributes to the pathogenesis of urticaria. This study aimed to assess the causal relationships between the genetically predicted urticaria subtypes and psychiatric disorders and further examined the role of GM in influencing the risk of these urticaria subtypes. METHODS: We conducted a meta-analysis of observational studies identified from four databases to evaluate the associations between urticaria, anxiety, and depression over the past decade. In addition, we estimated the genetic correlation and causality between genetically predicted urticaria subtypes and psychiatric disorders using linkage disequilibrium score regression and Mendelian Randomization (MR) analyses. Finally, univariable two-sample MR and multivariable MR analyses were employed to evaluate the combined and independent effects of GM from two datasets on urticaria subtypes associated with psychiatric disorders. RESULTS: Thirteen observational studies comprising 7321 participants were included in the meta-analysis. There was a positive association between urticaria and anxiety risk (n = 13, OR: 3.96; 95%CI: 2.90-5.41) as well as depression risk (n = 12, OR: 3.03; 95%CI: 2.30-4.01). The MR results indicated that idiopathic urticaria increased the risk of anxiety (OR = 1.14; 95%CI = 1.01-1.28; P = 3.31 × 10-2), while allergic urticaria increased the risk of major depressive disorder (OR = 1.07; 95%CI = 1.02-1.13; P = 6.65 × 10-3). Our analysis identified nineteen gut bacterial taxa that were causally associated with idiopathic and allergic urticaria. Notably, Intestinibacter and Victivallales were strongly associated with an increased risk of allergic urticaria, even after accounting for the effect of smoking or alcohol consumption in the multivariable MR analysis. FamilyXIIIAD3011group and Bacteroides vulgatus were found to exert protective roles in idiopathic urticaria. CONCLUSIONS: The study provides evidence for the association between urticaria subtypes and psychiatric disorders, complementing existing observational studies. In addition, our study implies the involvement of gut microbiota in idiopathic and allergic urticaria. However, the specific mechanisms of bacterial action remain to be clarified.
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The gut microbiota in post-stroke depression: A systematic review of microbial mechanisms and therapeutic targeting of neuroinflammation.
Post-stroke depression (PSD), a frequent and debilitating complication after stroke, severely hinders rehabilitation. Emerging evidence underscores the role of neuroinflammation and the gut microbiota in PSD pathogenesis. This review systematically elaborates the mechanisms by which gut dysbiosis contributes to PSD-related neuroinflammation via immune cell regulation (e.g., Treg/Th17 balance), microbial metabolites (e.g., SCFAs, tryptophan derivatives), and neural pathways (vagus nerve, HPA axis). A key focus is the comparative analysis of the gut microbiota in PSD against major depressive disorder (MDD) and Alzheimer's disease (AD), revealing a unique, stroke-induced microbial signature characterized by a loss of protective symbionts and a bloom of pro-inflammatory taxa. We further discuss the translational potential of microbiota-targeted interventions (e.g., probiotics, prebiotics) for PSD. By integrating clinical microbial ecology with mechanistic insights, this review synthesizes evidence suggesting that the gut microbiome may represent a promising diagnostic and therapeutic target for PSD, offering a distinct perspective from previous literature.